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Lamotrigine (LTG), a broad-spectrum anti-epileptic drug widely used in treatment for seizures, shows potential efficacy in Alzheimer’s disease (AD) therapy. Chronic LTG treatment rescues the suppressed long-term potentiation, loss of spines and cognitive deficits in AβPP/PS1 mice, known to overexpress a chimeric mouse/human mutant amyloid-β protein precursor (AβPP) and a mutant human presenilin 1 (PS1). These changes are accompanied by reduction of amyloid-β (Aβ) plaques density and of levels of β-C-terminal fragment of AβPP (β-CTF), a fragment of AβPP cleaved by β-secretase. These results suggest LTG treatment reduces Aβ production, possibly through modulation of cleavage of AβPP by β-secretase. However, the underlying mechanisms still remain unclear. In this study, decreased protein levels, but not mRNA levels of β-site AβPP-cleaving enzyme 1 (BACE1), were observed in cultured HEK293 …